Pulmonary Vascular Response to Nitroprusside in Dogs

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Although the effects of nitroprusside (NP) on myocardial function have been studied extensively, the effects of this vasodilator on the pulmonary vasculature have received less attention. In closed-chest anesthetized dogs, we used indicator dilution measurements of pulmonary blood volume (PBV), along-with measurements of pulmonary artery (Ppa) and left atrial (Pla) pressures, to address this problem in three experimental protocols. In protocol I, NP at 10-30 μg/kg per min in volume-expanded dogs reduced Ppa by 20% and Pla by 44% but produced no consistent change in PBV. In protocol II, NP at 1.8-5.4 μg/kg per min accompanied by autologous blood transfusion, sufficient to return Pla to the control level, resulted in no change in Ppa, but an increase in PBV from 8.8 to 9.9 ml/ kg (P < 0.05). In protocol m, NP at 2-6 μ/kg per min was compared to decreased venous return produced by partial occlusion of the inferior vena cava (TVC). With IVC occlusion adjusted to yield Pla equal to that during NP infusion, there was no difference in Ppa, but PBV was greater during NP infusion (10.5 ml/kg), compared to IVC occlusion (7.6 ml/kg, P < 0.05). In some experiments NP produced an increase in PBV when Pla and Ppa were reduced. In protocols II and m, NP decreased pulmonary vascular resistance by 40-50% (P < 0.05) at equal levels of Ppa. We conclude that NP shifts the pressure-volume curve of the pulmonary vasculature so that greater volume and flow are accommodated at the same pressure and, under some conditions, may produce a paradoxical increase in PBV while reducing pulmonary vascular pressure. Ore Res 45: 380-366, 1979

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